This research program addresses itself to the problem of the structure and function of vascular wall and cardiac cells and their reactions to injury. The problems of behavior of the cells of the artery wall and differences in the properties of the cells of human atherosclerotic plaques are being studied. The fact that atherosclerotic plaque cells in the human disease are clonal and its new implications for the causes and development of atherosclerosis are being explored in relation to operations of known and potental risk factors. The role of hypertension in modifying endothelial cell turnover is under investigation. How endothelial cells produce basal lamina and the mechanisms of platelet interaction with basal lamina are being investigated. The genesis of catecholamine-induced cardiomyopathy is being studied. How mast cells secrete biogenic amines, heparin and associated enzymes is being studied. The source of amyloid protein AA and the mechanisms by which it comes to be deposited in vascular walls and myocardium are being investigated. BIBLIOGRAPHIC REFERENCES: Vracko, R. and Benditt, E.P. Restricted replicative life-span of diabetic fibroblasts in vitro: its relationship to microangiopathy. Presented at the Conference "Biology of Development and Aging", Atlantic City, N.J., April 1974, Fed. Proc. 34:68-70, 1975. Eriksen, N., Ericsson, L.H., Pearsall, N., Lagunoff, D. and Benditt, E.P. Mouse amyloid protein AA: Homology with nonimmunoglobulin protein of human and monkey amyloid substance. Proc. Nat. Acad. Sci 73:964-967, 1976.